Background: The ability to scavenge reactive oxygen species (ROS) is crucial for cornea epithelial cells to resist oxidative damage. We previously demonstrated that exogenous thymosin beta-4 (Tb4) was able to protect human cornea epithelial (HCE-T) cells against H2O2-induced oxidative damage and its cellular internalization was essential. The aim of this study is to further elucidate its protective mechanism.
Methods: HCE-T cells with or without Tb4 pre-treatment were exposed to H2O2 and the differences in caspase activity, intracellular ROS levels, cell viability, and the expression of anti-oxidative enzymes, were measured and compared.
Results: Besides reducing caspase-9 activation and intracellular ROS levels induced by H2O2, treatment of Tb4 could also increase cell viability and stimulate the expression of manganese superoxide dismutase (SOD) and copper/zinc SOD. Moreover, both transcription and translation levels of catalase were also up-regulated by Tb4 in the presence of exogenous H2O2. Furthermore, it was demonstrated that the addition of catalase inhibitor abrogated the protective effect of Tb4 against H2O2-induced oxidative damage.
Conclusion: To our best knowledge, this is the first report to show that Tb4 was capable of up-regulating anti-oxidative enzymes in human corneal epithelial cells and our findings further support its role in cornea protection.